Chrysanthemum indicum. C. sinense 野 菊 花   Yě jú huā   Wild chrysanthemum flowers Family: Asteraceae 
PART USED: Dry inflorescence- harvested in Autumn when the flowers are blooming.
Nature: Cool, neutral, cold    FLAVOR: Bitter, acrid   CHANNEL: Lung, Liver
FUNCTIONS
GROUP: Exterior Clearing- Cooling
1. Clear Heat and Neutralize Toxins.[4,5] Clears fevers and detoxifies.[1]
2. Clear Liver Fire. Clear Wind Fire.[5]
3. Exterior clearing.
4. Eliminates moisture and reduces swelling.[1]
ACTIONS
INDICATIONS
1. Toxic Heat causing skin conditions:[4] Carbuncle. Skin nodules, scrofula. Sore and swollen throat,[5] also for influenza. Swelling from boils and abscesses.[1,4] Furuncles, carbuncles and sores.[5]
2. Liver Fire syndrome with eye congestion, photophobia and lacrimation and hyptertension with headache, irritability, and flushed face, wiry and rapid pulse. Red eyes with swelling and pain. Headache, vertigo. Wind Fire causing red eyes.[5]
3. Epidemic encephalomyelitis.[1]
4. Hypertension.[1,4]
CONTRAINDICATIONS: Preparations of Ye ju hua are extremely non-toxic. Except for occasional nausea and vomiting, there have been no adverse reactions or toxic properties reported.[5]
PATENT COMBINATIONS
COMBINATIONS
PREPARATIONS: Decoction. Dry inflorescence  9-15 g.[2,3,4] 6-12 g.[5] Also used externally as a compress or wash. Good quality is yellow, intact, aromatic, and bitter.

Whole plant 15-30 g. A suitable amount may be prepared for external use.[1]
HABITAT: Found growing wild everywhere.
DESCRIPTION: Wild Chrysanthemum is a perennial herb 1 m in height. Stems: clustered, with numerous branches, sparsely pubescent. Leaves; alternate, ovate or long-ovate, pinnately parted, apexes acute, bases cuneate, with stipules. Flowers: in autumn, terminal and axillary yellow flowers appear in corymb pattern forming racemose inflorescences. Fruit: an achene.
References
Inner Path can not take any responsibility for any adverse effects from the use of plants. Always seek advice from a professional before using a plant medicinally.
Constituents
Research

Safety Evaluation of Chrysanthemum indicum L. Flower Oil by Assessing Acute Oral Toxicity, Micronucleus Abnormalities, and Mutagenicity
Eun-Sun Hwang and Gun-Hee Kim
Abstract
Chrysanthemum indicum is widely used to treat immune-related and infectious disorders in East Asia. C. indicum flower oil contains 1,8-cineole, germacrene D, camphor, α-cadinol, camphene, pinocarvone, β-caryophyllene, 3-cyclohexen-1-ol, and γ-curcumene. We evaluated the safety of C. indicum flower oil by conducting acute oral toxicity, bone marrow micronucleus, and bacterial reverse mutation tests. Mortality, clinical signs and gross findings of mice were measured for 15 days after the oral single gavage administration of C. indicum flower oil. There were no mortality and clinical signs of toxicity at 2,000 mg/kg body weight/day of C. indicum flower oil throughout the 15 day period. Micronucleated erythrocyte cell counts for all treated groups were not significantly different between test and control groups. Levels of 15.63~500 μg C. indicum flower oil/plate did not induce mutagenicity in S. Typhimurium and E. coli, with or without the introduction of a metabolic activation system. These results indicate that ingesting C. indicum flower oil produces no acute oral toxicity, bone marrow micronucleus, and bacterial reverse mutation.
Prev Nutr Food Sci. 2013 Jun; 18(2): 111–116.
doi: 10.3746/pnf.2013.18.2.111
PMCID: PMC3892496 PMID: 24471119 ncbi.nlm.nih.gov

Anti-inflammatory components of Chrysanthemum indicum flowers.
Luyen BT, Tai BH, Thao NP, Cha JY, Lee HY, Lee YM, Kim YH.
Abstract
One new octulosonic acid derivative, chrysannol A (1), along with 17 known compounds (2-18), were isolated from Chrysanthemum indicum flowers. Their structures were determined from 1D NMR, 2D NMR, HR-ESI-MS spectral data, and comparisons with previous reports. The effects of these compounds on lipopolysaccharide (LPS)-induced nitric oxide (NO) and tumor necrosis factor alpha (TNF-α) production by RAW 264.7 cells were investigated. Compound 8 showed the highest inhibition of NO production of 46.09% at a concentration of 10.0μM. Compounds 7, 10, 11, and 16 inhibited TNF-α secretion at all concentration tested (0.4, 2.0, and 10.0μM), with inhibition values ranging from 22.27% to 33.13%. In addition, compound 8 and 9 decrease COX-2 and iNOS protein on Western blot analysis in dose dependent manner.
PMID: 25497988 DOI: 10.1016/j.bmcl.2014.11.054 Bioorg Med Chem Lett. 2015 Jan 15;25(2):266-9. doi: 10.1016/j.bmcl.2014.11.054. Epub 2014 Nov 27. ncbi.nlm.nih.gov

Chrysanthemum indicum ethanolic extract inhibits invasion of hepatocellular carcinoma via regulation of MMP/TIMP balance as therapeutic target.
Wang ZD, Huang C, Li ZF, Yang J, Li BH, Liang RR, Dai ZJ, Liu ZW.
Abstract
Hepatocellular carcinoma (HCC) is an aggressive cancer with a dismal outcome largely due to metastasis and postsurgical recurrence. Thus, the inhibition of invasion and metastasis is of great importance in its therapies. Medicinal plants or ethnopharmacology used in folklore medicine continue to be an important source of discovery and development of novel or potential therapeutic agents for treatment of cancer. Chrysanthemum indicum, one of the medicinal plants or ethnopharmacology, is being used for treatment of many diseases including cancer. However, this plant molecular mechanisms underlining the anti-metastatic effects have not been well documented. In this study, Chrysanthemum indicum ethanolic extract (CIE) significantly suppressed proliferation and invasion of MHCC97H cells, one of the HCC cell lines with high metastatic potential, in a dose-dependent manner. CIE markedly decreased MMP-2 and MMP-9 expression, increased simultaneously TIMP-1, and TIMP-2 expression further restoring their balance in the cancer cells. The present study indicates that CIE reduced MHCC97H cell metastatic capability, in part at least, through decrease of the MMP expression, simultaneous increase of the TIMP expression, further restoring their balance as therapeutic target in HCC. It is suggested that Chrysanthemum indicum is a potential novel therapeutic medicinal plant for treatment of HCC or cancer invasion and metastasis.
PMID: 20043102 Oncol Rep. 2010 Feb;23(2):413-21. ncbi.nlm.nih.gov

Chrysanthemum indicum L. extract induces apoptosis through suppression of constitutive STAT3 activation in human prostate cancer DU145 cells.
Kim C, Kim MC, Kim SM, Nam D, Choi SH, Kim SH, Ahn KS, Lee EH, Jung SH, Ahn KS.
Abstract
Chrysanthemum indicum L. has been shown to possess antiinflammatory and anticancer activities, but its molecular targets/pathways are not yet fully understood in tumor cells. In the present study, the potential effects of C. indicum on signal transducer and activator of transcription 3 (STAT3) signaling pathway in different tumor cells were examined. The solvent fractions (hexane, CH₂Cl₂, EtOAc, and BuOH,) were obtained from a crude extract (80% EOH extract) of C. indicum. The methylene chloride fraction of C. indicum (MCI) exhibited strong cytotoxic activity as compared with the other fractions and clearly suppressed constitutive STAT3 activation against both DU145 and U266 cells, but not MDA-MB-231 cells. The suppression of constitutive STAT3 activation by MCI is associated with blocking upstream JAK1 and JAK2, but not Src. MCI downregulated the expression of STAT3-regulated gene products; this is correlated with the accumulation of the cell cycle at sub-G1 phase, the induction of caspase-3 activation, and apoptosis. Moreover, the major components of the MCI were bioactive compounds such as sudachitin, hesperetin, chrysoeriol, and acacetin. Sudachitin, chrysoeriol, and acacetin also exerted significantly cytotoxicity, clearly suppressed constitutive STAT3 activation, and induced apoptosis, although hesperetin did not show any significant effect in DU145 cells. Overall, our results demonstrate that MCI could induce apoptosis through inhibition of the JAK1/2 and STAT3 signaling pathways.
PMID: 22438130 DOI: 10.1002/ptr.4689 Phytother Res. 2013 Jan;27(1):30-8. doi: 10.1002/ptr.4689. Epub 2012 Mar 22. ncbi.nlm.nih.gov